The inflammatory airway response in allergic asthma may be the result of immune cells that are dysregulated towards environmental factors such as airborne fungi. The long-term goal of this project is to better understand the pathophysiological mechanisms of Th2-type (allergic) airway inflammation. Exposure to the fungus, Alternaria, has long been implicated in the development and exacerbation of allergic airway disorders such as rhinitis, atopic asthma, and CRS. After intranasal exposure to Alternaria spores, antigens, and fungal cell wall polymers such as chitin, naive mice exhibit marked eosinophilic airway inflammation, enhanced Th2 responses, and airway hyperreactivity. Despite the well-documented clinical importance of Alternaria in the development, onset, and exacerbation of allergic airway diseases, little knowledge exists about the role of individual fungal products/components in theses pathological states. The importance of the fungal cell wall polymer chitin has been explored to some extent in the context of inflammation and has been shown to drive immune responses favoring the development of allergic disease. We have discovered a novel receptor candidate for chitin expressed in lung epithelial cells. In this exploratory project we will further our understanding of how chitin binds to this receptor and begin to elucidate the role of this receptor candidate in the context of innate immunity and allergic inflammatory responses using lung epithelial cells and mouse models. Execution of this project will lead to a better understanding of the mechanisms of persistent and recurrent airway inflammation and may lead to the development of more specific, effective therapies and prevention strategies.